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Biomedical subjects

S Ritter

Publications and source records attributed to S Ritter.

At least 145 records · Page 8Linked to original sources
PubMed1980

The antiaggressive effect of lithium is abolished by area postrema lesion.

Lithium (Li) suppresses intraspecific aggression in rats and other mammals. However, antiaggressive doses of Li have been shown to produce signs of illness and to serve as an unconditioned stimulus for conditioned taste aversions (CTA). Therefore, it is possible that the antiaggressive effects of Li result from Li-induced malaise. Malaise and CTA's produced by some drugs and toxins are mediated by chemoreceptors in the area postrema. In this paper we report [1] that thermal lesion of the area postrema abolishes Li's ability to condition taste aversions and [2] that area postrema lesion abolishes the antiaggressive effect of Li as measured by attack latency in a shock-induced aggression test. Taken together, these findings suggest that some or all of Li's antiaggressive action in rats may result from malaise attributable to Li's action on the area postrema.

Aggression↗
PubMed1978

Absence of glucoprivic feeding after stress suggest impairment of noradrenergic neuron function.

Feeding in response to 2-deoxy-D-glucose (2DG), a quantifiable behavior which appears to depend on noradrenergic (NE) neuron function, was used in these experiments to evaluate the functional capabilities of NE neurons after stress exposure. Depletion of hypothalamic NE after footshock or hypothermic stress was directly correlated with impairment of glucoprivic feeding. When NE depletion was prevented by prior exposure to chronic stress, no impairment of feeding was observed. After hypothermic stress, repletion of NE proceeded more rapidly in the telencephalon than in the hypothalamus and reappearance of a normal feeding response precisely paralleled the time course of repletion in the hypothalamus. Drinking in response to cell dehydration, a behavior not directly dependent on brain catecholamines, was not impaired after either footshock or hypothermic stress, despite similar NE depletions. Presence of a normal drinking response assured that deficits observed in the 2DG test were not due to nonspecific behavioral suppression resulting from stress. These data suggest that NE neuron function may be impaired or temporarily abolished after severe stress exposure. In addition, these results demonstrate that behavioral pathology need not be the result of massive neurotransmitter depletion but may result from relatively subtle alterations of specific neurotransmitter pools.

Animals↗
PubMed1977

Studies on derivatives of phenyltetrahydrofuranone-2-carboxylic acids. VI. Derivatives of beta-phenyltetrahydrofuranone-2-beta-carboxylic acid.

Proceeding with the studies on derivatives of pheyl-tetrahydrofuranone-2-carboxylic acids the authors have stated that the reaction of hydroxymethylation of ethyl ester of beta-phenyl-beta-cyanopropionic acid I gives transitionally beta-phenyl-beta-cyano-beta-hydroxymethylpropionic acid II which, after a long time, transforms into an amide of beta-phenyl-tetrahydrofuranone-2-beta-carboxylic acid (III). Amide III is tranformed, through acid IV, into acid chloride V that gives a number of derivatives: amide III, substituted amides (VI-IX), methyl ester X, ureide XI, and aminomethylamides (XII, XIII). The chemical structure of these compounds has been confirmed by elemental analysis and IR and PMR spectra. The compounds newly obtained were invested pharmacologically. It has been found that some of the derivatives (III, VI, VII, VIII, XII, XIII) exert a depressing action on the central nervous system.

Central Nervous System↗
PubMed1975

Neurochemical regulation of feeding in the rat: facilitation by alpha-noradrenergic, but not dopaminergic, receptor stimulants.

Rats ate voraciously after intraventricular injections of the alpha-noradrenergic receptor stimulant clonidine. Intraventricular administration of l-norepinephrine also facilitated feeding, but similar injections of dopamine and apomorphine (a dopamine receptor stimulant) were ineffective and even tended to suppress feeding. Clonidine was 100 times more potent than norepinephrine and increased the intake of both the ordinary diet of powdered food and a highly palatable wet food. The anorexic action of amphetamine was reversed by centrally administered clonidine. These observations suggest "respondent" rather than "operant" regulation of feeding by noradrenergic systems. That is, in relation to noradrenergic mechanisms, feeding appears to be a respondent which is sensitized or disinhibited by activation of alpha-noradrenergic receptors, rather than an operant which is reinforced by the release of norepinephrine.

Adrenergic alpha-Agonists↗